A tachycardia is a very rapid rhythm or rate of the heart. In recent years, with the advent of multi-mode dual-chamber demand-type cardiac pacemakers, it has been discovered that the pacemaker itself, in responding to sensed electrical activity in the heart (which electrical activity may be premature or the result of retrograde conduction) may be responsible, at least in part, for triggering and/or maintaining a tachycardia in those patients who have retrograde conduction. In such an instance, the resulting tachycardia is referred to as a pacer mediated tachycardia (PMT) because it is the operation of the pacemaker that sustains the tachycardia, typically at the maximum tracking rate of the pacemaker.
In order to efficiently perform its function of a pump, the heart must maintain a natural AV synchrony. The term "AV syncrony" relates to the sequential timing relationship that exists between the contractions of the atria and the ventricles. In a given heart cycle or beat, these contractions are typically manifest or measured by sensing electrical signals or waves that are attendant with the depolorization of heart tissue, which depolorization immediately precedes (and for most purposes can be considered concurrent with) the contraction of the cardiac tissue. These signals or waves can be viewed on an electrocardiogram and include a P-wave, representing the depolorization of the atria; the QRS wave (sometimes referred to as an R-wave, the predominant wave of the group), representing the depolorization of the ventricles; and the T-wave, representing the repolarization of the ventricles. (It is noted that the atria also are repolarized, but this atrial repolarization occurs at approximately the same time as the depolorization of the ventricles; and any electrical signal generated by atrial repolarization is generally minute masked out by the much larger QRS-wave on the electrocardiogram.)
Thus, it is the P-QRS-T cycle of waves that represents the natural AV synchrony of the heart. These waves, including the timing relationships that exist therebetween, are carefully studied and monitored through conventional ECG techniques whenever the operation of the heart is being examined.
Multiple-mode, dual-chamber, demand-type, cardiac pacemakers are designed, insofar as possible, to maintain an AV syncrony for damaged or diseased hearts that are unable to do so on their own. This is realized by placing electrodes in both the right atrium and right ventricle of the heart. These electrodes are coupled through intravenous and/or epicardial leads to sense amplifiers housed in an implanted pacemaker. Electrical activity occurring in these chambers can thus be sensed. When electrical activity is sensed, the pacemaker assumes that a depolorization or contraction of the indicated chamber has occurred. If no electrical activity is sensed within a prescribed time interval, typically referred to as an atrial or ventricular escape interval, then a pulse generator, also housed within the pacemaker housing, generates a stimulation pulse that is delivered to the indicated chamber, usually via the same lead or electrode as is used for sensing. This stimulation pulse causes or forces the desired depolorization and contraction of the indicated chamber to occur. Hence, by first sensing whether a natural depolorization occurs in each chamber, and by second stimulating at controlled time intervals each chamber with an external stimulation pulse in the absence of a natural depolorization, the AV synchrony of the heart can be maintained.
Unfortunately, there are many operating constraints and conditions of the heart that complicate the operation of a demand-type pacemaker. (A demand-type pacemaker is one that provides a stimulation pulse only when the heart fails to produce a natural depolorization on its own within a prescribed escape interval.) For example, there are certain time periods following a depolorization of cardiac tissue (prior to repolarization) when the application of an external electrical impulse is ineffective--that is, it serves no useful purpose, and thus represents an unneeded expenditure of the pacemaker's limited energy. Therefore the application of stimulation pulses during these time periods is to be avoided. Further, it is not uncommon for extraneous electrical signals or noise to be present. These electrical noise signals may be of sufficient amplitude to be sensed by the sensing amplifiers of the pacemaker, which sensing can "fool" the pacemaker into thinking that it has sensed electrical activity associated with a natural depolorization of the heart tissue, when in fact all that it has sensed is noise.
In order to prevent the pacemaker from generating and delivering stimulation pulses during the natural refractory time period of the heart, or from sensing and responding to electrical noise, it is common in the art to include within the pacemaker a timer circuit that defines a refractory period immediately subsequent to the sensing of major electrical activity, or immediately subsequent to the generating of an electrical stimulus. During this pacer-controlled refractory period, all of the sensing and pulse generating circuits of the pacemaker are inoperable. Following this refractory period, the sensing and pulse generating circuits are again operable and the normal sensing/pacing functions of the pacemaker continue.
One of the conditions of the heart that complicates the operation of a pacemaker is the occurrence of a premature ventricular contraction, or PVC. A PVC is a ventricular contraction that occurs out of sequence, i.e., after a previous ventricular contraction but prior to a succeeding atrial contraction. Needless to say, a recurring PVC may greatly disrupt the AV synchrony of the heart. Moreover the occurrence of an isolated PVC--an occurrence that is quite common--may, if a pacemaker is employed, "fool" the pacemaker into responding as though the PVC were a normal ventricular contraction. This is not all bad, inasmuch as any ventricular contraction, premature or otherwise, represents a major cardiac event from which most timing functions of the pacemaker are appropriately referenced. However, as set forth below, unless some sort of precautionary measures are taken, the occurrence of a PVC can combine with the otherwise normal operation of a dual chamber, multi-mode pacemaker operating in either the DDD or VDD mode of operation to trigger a pacer mediated tachycardia, or PMT.
To understand how a PMT may be triggered by the single occurrence of a PVC, it is necessary to have a basic understanding of retrograde conduction. Retrograde conduction is a condition of the heart whereby an impulse resulting from a spontaneous or paced contraction of the ventricle propagates or conducts into the atrium where it causes an atrial depolorization. This ventricle-to-atrium (VA) type of conduction is backwards from the normal atrium-to-ventricle (AV) type of conduction that occurs within the heart during normal operation, hence the term "retrograde" is employed to describe it.
When a PVC occurs in a patient having a pacemaker, it is quite possible that through retrograde conduction the PVC will also cause the atrium to contract a short time thereafter. The pacemaker, sensing the electrical activity of the atrium, responds to this retrograde atrial contraction as though it were a normal atrial contraction in a regular cardiac sequence. That is, in response to the sensed atrial activity which the pacemaker assumes is a natural or sinus P-wave, the pacemaker may generate a ventricular stimulation pulse for delivery to the ventricle a prescribed time period later, designated as the A-V time period, (which A-V time period, for purposes herein, may be extended by an appropriate factor to deal with Wenckeback behavior). This ventricular stimulation pulse causes the ventricle to contract at a time much earlier in the cardiac cycle than it would have otherwise. In the presence of retrograde conduction, a stimulating impulse resulting from this ventricular contraction may conduct into the atrium and cause an atrial contraction, and the whole process repeats itself, thereby causing a tachycardia or rapid heart rhythm truly mediated by the pacemaker. The mechanism that sustains this tachycardia or rapid heart rhythm is: ( 1) the retrograde path from the ventricle to the atrium, causing the atrium to contract a short time after every ventricular contraction, and (2) the anterograde or forward path from the atrium to the ventricle, provided by the pacemaker, causing the ventricle to receive a stimulation pulse a prescribed time subsequent to the contraction of the atrium. As explained previously, this type of tachycardia, wherein one of the paths that sustains it is provided by the pacemaker, is referred to as a pacer mediated tachycardia, or PMT. Disadvantageously, as is evident from the description given above, under the right circumstances the occurrence of a single PVC can trigger a PMT. A PMT is typically characterized by the heart beating at its maximum tracking rate as set by the pacemaker. (Note: all dual chamber pacemakers which track atrial events typically employ timing circuits that set an upper limit at which pacing pulses will be provided. This upper limit, referred to as the maximum tracking rate, is the rate at which a PMT is generally sustained, although in some instances the rate of a PMT may be lower than the maximum tracking rate.)
To prevent a PVC from triggering a PMT, it is known in the art to extend the pacemaker-generated atrial refractory period upon detection of a PVC. That is, if a PVC is defined as a sensed ventricular event that occurs prior to an atrial event in the normal cardiac cycle, then the logic circuits of the pacemaker can detect when a PVC occurs. Upon such detection, the atrial refractory period, present in each cardiac cycle, is automatically extended a prescribed amount. For example, the Cosmos pacer manufactured by Intermedics, Inc. of Freeport, Tex., extends the atrial refractory period by a programmable amount upon the sensing of each PVC. Similarly, the AFP pacemaker manufactured by Pacesetter Systems, Inc., of Sylmar, Calif., extends the atrial refractory period by a fixed extension period that is equal to the entire remaining interval within the cardiac cycle. The reason for extending the atrial refractory period, as taught in the art, is to prevent the subsequent retrograde atrial depolarization, if present, from being sensed, thereby "controlling" the pacemaker to operate as though no atrial activity had occurred. This means that the next event in the cardiac cycle following the ventricular contraction would be the generation of an atrial stimulus. The teachings of the art are that the extension of the atrial refractory period should be extended a sufficient amount so that any retrograde atrial event will fall within this extension, thereby precluding such retrograde atrial event from being sensed.
Unfortunately, it has recently been learned that extension of the atrial refractory period can itself create the conditions necessary to start a PMT. For example, the occurrence of a PVC, which occurrence causes the atrial refractory period to be extended, may not cause a retrograde atrial contraction. If such is the case, there is a chance that a natural or sinus P-wave will fall near the end of the extended atrial refractory period. However, this P-wave will not be sensed by the pacemaker because it occurs during the pacer-defined refractory time period. Hence, the pacemaker continues to operate as though no sinus P-wave had occurred, generating an atrial stimulus, followed by a ventricular stimulus one A-V delay later. However, the atrial stimulus may not be effective due to the natural refractory period of the heart as a result of the nonsensed sinus P-wave. This results in an effective prolongation of the A-V delay (sinus P-wave to paced ventricular stimulus), which prolongation enhances the likelihood that retrograde conduction will occur. If retrograde conduction is present at the subsequent ventricular stimulus, a PMT may be started. Because of this possibility there is a need in the art for a pacemaker response to a PVC that reduces the likelihood of triggering a PMT.
Other mechanisms exist for triggering a PMT besides a PVC, such as tracking of electrical signals produced by muscle movement (myopotentials) or premature atrial contractions. Accordingly, there is also a need in the pacemaker art for a means of breaking a PMT once started. One approach known in the art for breaking a PMT is to drop one ventricular stimulus for every 16 beats at the maximum tracking rate. While this may be effective in some instances, it is not always effective. For example, as used in the art, a ventricular stimulus is dropped only when the pacemaker is operating at its maximum tracking rate. While the preponderance of PMT cases are at the maximum tracking rate, it is conceivable that a PMT could occur at a different rate. Further, by dropping the ventricular stimulus completely and going an additional full cycle, the pause in ventricular stimulus becomes sufficiently long so as to increase the possibility of another PVC. This PVC may then again immediately restart the PMT that was just terminated.